Acute Pancreatitis Presenting as Sudden, Unexpected Death

Institute of Legal Medicine and Forensic Sciences, Berlin, Germany.
American Journal of Forensic Medicine & Pathology (Impact Factor: 0.7). 10/2007; 28(3):267-70. DOI: 10.1097/PAF.0b013e3181425615
Source: PubMed


Acute pancreatitis represents a spectrum of disease, ranging from a mild, transitory illness to a severe, rapidly progressive hemorrhagic form, with massive necrosis and mortality rates of up to 24%. The reported incidence of acute pancreatitis diagnosed first at clinicopathologic autopsy ranges between 30% and 42%. To better describe outpatient fatalities due to acute pancreatitis that present as sudden, unexpected death, we retrospectively reviewed the autopsy files at the Institute of Legal Medicine, University of Hamburg, Germany, from 2000-2004. Individual cases were analyzed for sex, age, race, circumstances of death, social background of the deceased and previous medical history, seasonal occurrence of the disease, blood alcohol concentration at the time of death, body mass index, autopsy findings, histopathology, and etiology of acute pancreatitis. Among the 6178 autopsies carried out during the 5-year period evaluated, there were 27 cases of acute pancreatitis that presented as sudden, unexpected death. In all cases, the diagnosis was first made at autopsy. The male:female ratio was 1.7:1 and the mean age was 52 years (range, 30-91 years). Etiologies of acute pancreatitis included alcohol (n=19), gall stones (n=2), other identified etiologic factors (n=3), and idiopathic (n=3). Complications of acute pancreatitis included lung edema and/or acute respiratory distress syndrome, peritonitis, disseminated intravascular coagulation, and sepsis. At least 20 subjects (74%) had lived isolated, with no social contacts. Contrary to the clinical observations of a clear seasonal variation in the onset of acute pancreatitis, we found no correlation between death due to acute pancreatitis and a specific month or season. Many prior studies have suggested that the majority of deaths in severe acute pancreatitis occur in the late phase of the disease as a result of pancreatic sepsis. Conversely, in the present study, the majority of affected individuals died during the very early phase of the disease. While gallstones represent the main etiologic factor in most larger clinical series, biliary etiology seems to play only a minor role in outpatient deaths undergoing medicolegal autopsies. Data derived from medicolegal autopsy studies should be included in future population-based studies of acute pancreatitis.

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    ABSTRACT: Acute pancreatitis (AP) is a common disease. Mild disease resolves spontaneously in a few days. Severe forms of the disease can lead to local complications, necrosis, and abscesses in and around the pancreas. Systemic inflammation in severe AP is associated with distant organ failures. The aim of this study is to identify genetically determined prognostic factors involved in the clinical features of AP. The study employs a candidate-gene approach, and the genes are involved in trysinogen activation in the initiation phase of the disease, as well as in the systemic inflammation as the disease proceeds. The last study examines adipokines, fat-derived hormones characterized with the capacity to modify inflammation. SPINK 1 is a gene coding trypsin activation inhibitor. Mutations N34S and P55N were determined by minisequencing methods in 371 AP patients and in 459 controls. The mutation N34S was more common in AP patients (7.8%) than in controls (2.6%). This suggests that SPINK 1 gene mutation N34S is a risk factor for AP. In the fourth study, in 12 matched pairs of patients with severe and mild AP, levels of adipokines, adiponectin, and leptin were evaluated. Plasma adipokine levels did not differ between patients with mild and severe AP. The results suggest that in AP, adipokine plasma levels are not factors predisposing to organ failures. This study identified the SPINK 1 mutation N34S to be a risk factor for AP in the general population. As AP is a multifactorial disease, and extensive genetic heterogeneity is likely, further identification of genetic factors in the disease requires larger future studies with more advanced genetic study models. Further identification of the patient characteristics associated with organ failures offers another direction of the study to achieve more detailed understanding of the severe form of AP. Akuutti haimatulehdus on tavallinen akuutin vatsakivun syy. Lievä haimatulehdus paranee muutamassa päivässä. Vaikeaan haimatulehdukseen liittyy paikallisia komplikaatioita; kudoskuoliota ja paiseita haimassa ja sen ympärillä ja systeeminen tulehdusreaktio liittyy monielinvaurioon. Tämän tutkimuksen tarkoituksena on tunnistaa geneettisesti määräytyviä ennusteellisia tekijöitä akuutissa haimatulehduksessa. Tutkimuksen kandidaattigeenit liittyvät trypsinogeenin aktivaatioon taudin alussa ja systeemiseen tulehdukseen taudin edetessä. Viimeinen osatyö tutkii adipokiinien mahdollista osuutta systeemisen tulehduksen säätelijöinä. SPINK 1 koodaa trypsiinin aktivaation inhibiittoria. Tämän geenin mutaatiot N34S ja P55N määritettiin minise-kvensoimalla 371 akuuttia haimatulehdusta sairastavalta potilaalta ja 459 kontrollihenkilöltä. Mutaatio N34S oli tavallisempi akuuttia haimatulehdusta sairastavilla potilailla (7.8%) kuin kontrolleilla (2.6%). Tulehdusgeenipolymorfismit geeneissä TNF, HSPA1B, CD14 and IL-10 on liitetty kirjallisuudessa alkoholi-haimatulehduksen riskiin ja siihen että haimatulehdus kehittyy vaikeaksi. Tutkimuksen 397 akuuttia haimatulehdusta sairastaneelta potilaalta ja 310 kontrollihenkilöltä määritettiin genotyypit MALDI-TOF tekniikkaan perustuvalla menetelmällä. Eroja eri tutkimusryhmien välillä ei todettu. Hemostaattisen muutokset liittyvät tulehdukseen ja hyytymistä edistävät tekijät saattavat vahventaa tulehdusreak-tioita. Hyytymistä edistävä hyytymistekijä V Leiden mutaatio ja plasminogeenin aktivaation inhibiittori -1 4G/5G polymorfia määritettiin 397 haimatulehduspotilaalta ja 310 kontrollihenkilöltä. Tutkimusaineistossa näiden po-lymorfioiden alleelifrekvenssit eivät eronneet kontrolliaineistosta. Neljännessä osatyössä tutkittiin adipokiinien, adipokiinin ja leptiinin pitoisuuksia plasmassa lievää ja vaikeaa haimatulehdusta sairastavilla potilailla. Sairaalaan tulovaiheessa ei todettu eroja plasman adipokiini pitoisuuksissa potilailla joilla oli lievä tai vaikea akuutti haimatulehdus. Tuloksista voidaan päätellä että adipokiinit eivät vaikuta systeemiseen tulehdukseen akuutissa haimatulehduksessa. Tämän väitöskirjatyön tulokset osoittavat, että SPINK1 N34S mutaatio on riskitekijä akuuttiin haimatulehdukseen sairastumisessa. Akuutti haimatulehdus on monitekijäinen tauti ja taudin kulkuun vaikuttavien geneettisten tekijöiden tunnistaminen vaatii suuren potilasmäärän omaavia tutkimuksia ja tarkkaa tuntemusta muista tekijöistä jotka vaikuttavat taudin vaikeusasteeseen.
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    ABSTRACT: In the investigation of sudden death in adults, channelopathies, such as long QT syndrome, have risen to the fore in the minds of forensic pathologists in recent years. Examples of these disorders are touched upon in this review as an absence of abnormal findings at postmortem examination is characteristic and the importance of considering the diagnosis lies in the heritable nature of these conditions. Typically, a diagnosis of a possible channelopathy is evoked as an explanation for a 'negative autopsy' in a case of apparent sudden natural death. However, the one potential adverse effect of this approach is that subtle causes of sudden death may be overlooked. The intention of this article is to review and discuss potential causes of sudden adult death (mostly natural) that should be considered before resorting to a diagnosis of possible channelopathy. Nonetheless, it becomes apparent that many of the potential causes of sudden death can have a genetic basis. Thus, it becomes an important consideration that there may be a genetic basis to sudden death that extends beyond the negative autopsy.
    Forensic Science Medicine and Pathology 08/2009; 5(3):210-32. DOI:10.1007/s12024-009-9099-3 · 1.98 Impact Factor
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    ABSTRACT: Mortality caused by acute pancreatitis in patients admitted to the hospital has been thoroughly investigated, but knowledge regarding outpatient fatalities is far from complete. The purpose of this study was to assess the incidence and clinical characteristics of patients who have died due to acute pancreatitis occurring outside the hospital. Deaths caused by acute pancreatitis in the southern part of Sweden during 1994-2008 were identified at the Department of Forensic Medicine, Lund. A retrospective review of all cases was performed. A total of 50 patients were included, representing approximately 50 of 292 (17%) of all deaths due to acute pancreatitis in the region during this period of time. Median age was 54 (47-69) years and the majority-37 (74%)-were men. The main etiology was alcohol, seen in at least 35 (70%) patients. Twelve (24%) patients were obese. The duration of abdominal pain, in evaluable cases, was 3.0 (1.6-6.2) days. Profound signs of pancreatitis were seen in all patients; 35 (70%) had a necrotising disease according to histopathological examination. Pulmonary changes were common, e.g., bronchopneumonia, pleural effusion, or edema, and all but four had fatty liver. Massive intra-abdominal bleeding was seen in one patient. At least eight patients had a mental disorder, and three were homeless. Fatal acute pancreatitis occurring outside the hospital accounts for a substantial part of all deaths due to the disease. The incidence seems to decline, and no variation in season was seen. Alcohol was the predominant etiology. Many of the patients lived alone and in poor social conditions.
    World Journal of Surgery 10/2010; 34(10):2286-91. DOI:10.1007/s00268-010-0693-z · 2.64 Impact Factor
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